TY - JOUR
T1 - Differential hemodynamic and sympathoadrenal effects of sodium nitroprusside and hydralazine in hypertensive subjects
AU - Shepherd, Alexander M.M.
AU - Irvine, Norman A.
PY - 1986/5
Y1 - 1986/5
N2 - The hemodynamic and sympathoadrenal effects of serial incremental doses of a mixed veno-arte-riolar dilator (intravenous sodium nitroprusside 0.0125-0.50 μg/kg/min) and a pure arteriolar dilator (bolus injections of hydralazine, 0.05-0.3 mg/kg) were compared in 18 subjects with uncomplicated essential hypertension. Blood pressure was reduced to the same extent over approximately the same time with both drugs. Sodium nitroprusside produced significant reduction in cardiac output (9%) and stroke volume (16%) despite an 11% increase in heart rate. Total peripheral resistance did not change. In contrast, hydralazine produced a significant (39%) reduction in peripheral resistance with a compensatory increase in heart rate (19%), stroke volume (20%), and cardiac output (42%). The catecholamine responses to the drugs differed both quantitatively and qualitatively. Administration of both drugs was associated with gradual increases in plasma norepinephrine, but the levels were consistently 40% higher with sodium nitroprusside for the same fall in blood pressure. No consistent change in plasma epinephrine was found with sodium nitroprusside, whereas with hydralazine, the concentration increased gradually after the blood pressure had been reduced by 9 mm Hg. This threshold was independent of the starting blood pressure. These differences in catecholamine response could reflect different patterns of regional sympathetic activation by the low pressure mechanoreceptors (sodium nitroprusside) and by the arterial baroreceptors (hydralazine). Neither drug has an ideal hemodynamic profile, particularly in subjects with cardiac disease, but a balanced combination of the two may produce a favorable hemodynamic profile and optimal hypotensive effect, minimizing the need for large doses of sympathetic inhibitors.
AB - The hemodynamic and sympathoadrenal effects of serial incremental doses of a mixed veno-arte-riolar dilator (intravenous sodium nitroprusside 0.0125-0.50 μg/kg/min) and a pure arteriolar dilator (bolus injections of hydralazine, 0.05-0.3 mg/kg) were compared in 18 subjects with uncomplicated essential hypertension. Blood pressure was reduced to the same extent over approximately the same time with both drugs. Sodium nitroprusside produced significant reduction in cardiac output (9%) and stroke volume (16%) despite an 11% increase in heart rate. Total peripheral resistance did not change. In contrast, hydralazine produced a significant (39%) reduction in peripheral resistance with a compensatory increase in heart rate (19%), stroke volume (20%), and cardiac output (42%). The catecholamine responses to the drugs differed both quantitatively and qualitatively. Administration of both drugs was associated with gradual increases in plasma norepinephrine, but the levels were consistently 40% higher with sodium nitroprusside for the same fall in blood pressure. No consistent change in plasma epinephrine was found with sodium nitroprusside, whereas with hydralazine, the concentration increased gradually after the blood pressure had been reduced by 9 mm Hg. This threshold was independent of the starting blood pressure. These differences in catecholamine response could reflect different patterns of regional sympathetic activation by the low pressure mechanoreceptors (sodium nitroprusside) and by the arterial baroreceptors (hydralazine). Neither drug has an ideal hemodynamic profile, particularly in subjects with cardiac disease, but a balanced combination of the two may produce a favorable hemodynamic profile and optimal hypotensive effect, minimizing the need for large doses of sympathetic inhibitors.
KW - Hemodynamics
KW - Hypertension
KW - Plasma catecholamines
KW - Vasodilators
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U2 - 10.1097/00005344-198605000-00014
DO - 10.1097/00005344-198605000-00014
M3 - Article
C2 - 2425168
AN - SCOPUS:0022912488
VL - 8
SP - 527
EP - 533
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
SN - 0160-2446
IS - 3
ER -